Study on the Application of Kramers-Kronig Relation for Polyurethane Mixture.

Polyurethane (PU) mixture, which is a new pavement mixture, exhibits different dynamic properties compared to a hot-mixed asphalt mixture (HMA). This paper analyzed whether the Kramers-Kronig (K-K) relation and thermorheologically simple properties applied to the PU mixture. Based on the results, the PU mixture exhibited thermorheologically simple properties within the test conditions. The time-temperature superposition principle (TTSP) was applicable for the PU mixture to construct a dynamic modulus master curve using the standard logistic sigmoidal (SLS) model, the generalized logistic sigmoidal (GLS) model, and the Havriliak-Negami (HN) model. The Hilbert integral transformed SLS and GLS models for the phase angle can accurately fit the measured phase angle data with newly fitted shift factors and predict the phase angle within the viscoelastic range. The core-core and black space diagrams both displayed single continuous smooth curves, which can be utilized to characterize the viscoelastic property of the PU mixture. The K-K relation is applicable for the PU mixture to obtain the phase angle master curve model, storage modulus, and loss modulus from the complex modulus test results with the test temperatures and loading frequencies. The phase angle of the PU mixture at extremely high or low test temperatures cannot be derived from the dynamic modulus data.

Enhancement of ionospheric heating effect by chemical release.

The ionosphere can be artificially modified by employing ground-based high-power high-frequency electromagnetic waves to irradiate the ionosphere. This modification is achieved through the nonlinear interaction between the electromagnetic waves and the ionospheric plasma, leading to changes in the physical properties and structure of the ionosphere. The degree of artificial modification of the ionosphere is closely related to the heating energy density of high-frequency pump waves. Due to the high density of neutral constituents in the lower ionosphere and the high frequency of electron-neutral collisions, the energy of heating pump waves will be absorbed and attenuated during the penetration of the low ionosphere, seriously affecting the heating effect. This paper proposes a method to reduce the absorption of ionospheric heating pump waves by releasing electron attachment chemicals into low ionosphere to form a large-scale electron density hole. A model for mitigating pump waves absorption based on SF6 release is established, and the absorption at different frequencies is quantitatively calculated. The propagation characteristics of high-frequency signals in ionospheric holes are studied using a three-dimensional ray tracing method, and the results demonstrate that the chemical release method not only reduces the absorption attenuation of heating pump waves but also forms spherical electron density holes, which exhibit a focusing effect on the heating beam and enhance the heating effect. The results are of great significance for understanding the nonlinear interaction between electromagnetic wave and ionospheric plasma and improving the ionospheric heating efficiency.

Limit state equation and failure pressure prediction model of pipeline with complex loading.

Assessing failure pressure is critical in determining pipeline integrity. Current research primarily concerns the buckling performance of pressurized pipelines subjected to a bending load or axial compression force, with some also looking at the failure pressure of corroded pipelines. However, there is currently a lack of limit state models for pressurized pipelines with bending moments and axial forces. In this study, based on the unified yield criterion, we propose a limit state equation for steel pipes under various loads. The most common operating loads on buried pipelines are bending moment, internal pressure, and axial force. The proposed limit state equation for intact pipelines is based on a three-dimensional pipeline stress model with complex load coupling. Using failure data, we investigate the applicability of various yield criteria in assessing the failure pressure of pipelines with complex loads. We show that the evaluation model can be effectively used as a theoretical solution for assessing the failure pressure in such circumstances and for selecting appropriate yield criteria based on load condition differences.

Gut microbiota and neuropsychiatric disorders: Implications for neuroendocrine-immune regulation.

Recently, increasing evidence has shown gut microbiota dysbiosis might be implicated in the physiological mechanisms of neuropsychiatric disorders. Altered microbial community composition, diversity and distribution traits have been reported in neuropsychiatric disorders. However, the exact pathways by which the intestinal microbiota contribute to neuropsychiatric disorders remain largely unknown. Given that the onset and progression of neuropsychiatric disorders are characterized with complicated alterations of neuroendocrine and immunology, both of which can be continually affected by gut microbiota via "microbiome-gut-brain axis". Thus, we assess the complicated crosstalk between neuroendocrine and immunological regulation might underlie the mechanisms of gut microbiota associated with neuropsychiatric disorders. In this review, we summarized clinical and preclinical evidence on the role of the gut microbiota in neuropsychiatry disorders, especially in mood disorders and neurodevelopmental disorders. This review may elaborate the potential mechanisms of gut microbiota implicating in neuroendocrine-immune regulation and provide a comprehensive understanding of physiological mechanisms for neuropsychiatric disorders.

GABAergic System Dysfunction in Autism Spectrum Disorders.

Autism spectrum disorder (ASD) refers to a series of neurodevelopmental diseases characterized by two hallmark symptoms, social communication deficits and repetitive behaviors. Gamma-aminobutyric acid (GABA) is one of the most important inhibitory neurotransmitters in the central nervous system (CNS). GABAergic inhibitory neurotransmission is critical for the regulation of brain rhythm and spontaneous neuronal activities during neurodevelopment. Genetic evidence has identified some variations of genes associated with the GABA system, indicating an abnormal excitatory/inhibitory (E/I) neurotransmission ratio implicated in the pathogenesis of ASD. However, the specific molecular mechanism by which GABA and GABAergic synaptic transmission affect ASD remains unclear. Transgenic technology enables translating genetic variations into rodent models to further investigate the structural and functional synaptic dysregulation related to ASD. In this review, we summarized evidence from human neuroimaging, postmortem, and genetic and pharmacological studies, and put emphasis on the GABAergic synaptic dysregulation and consequent E/I imbalance. We attempt to illuminate the pathophysiological role of structural and functional synaptic dysregulation in ASD and provide insights for future investigation.

Changes in Hippocampal Plasticity in Depression and Therapeutic Approaches Influencing These Changes.

Depression is a common neurological disease that seriously affects human health. There are many hypotheses about the pathogenesis of depression, and the most widely recognized and applied is the monoamine hypothesis. However, no hypothesis can fully explain the pathogenesis of depression. At present, the brain-derived neurotrophic factor (BDNF) and neurogenesis hypotheses have highlighted the important role of plasticity in depression. The plasticity of neurons and glial cells plays a vital role in the transmission and integration of signals in the central nervous system. Plasticity is the adaptive change in the nervous system in response to changes in external signals. The hippocampus is an important anatomical area associated with depression. Studies have shown that some antidepressants can treat depression by changing the plasticity of the hippocampus. Furthermore, caloric restriction has also been shown to affect antidepressant and hippocampal plasticity changes. In this review, we summarize the latest research, focusing on changes in the plasticity of hippocampal neurons and glial cells in depression and the role of BDNF in the changes in hippocampal plasticity in depression, as well as caloric restriction and mitochondrial plasticity. This review may contribute to the development of antidepressant drugs and elucidating the mechanism of depression.

Effects of Electroconvulsive Therapy on Depression and Its Potential Mechanism.

Depression is one of the most common disorders causing mortality around the world. Although electroconvulsive therapy (ECT) is, along with antidepressants and psychotherapy, one of the three major treatments of depression, it is still considered as the last resort for depressed patients. This situation is partially due to limited studies and uncertainty regarding its mechanism. However, decades of increased research have focused on the effects of ECT on depression and its potential mechanism. Furthermore, these investigations may suggest that ECT should be a first-line therapy for depression due to its profound effects in relieving desperation in certain situations. Here, we outline recent clinical and preclinical studies and summarize the advantages and disadvantages of ECT. Thus, this review may provide some hints for clinical application.

Role of Leptin in Mood Disorder and Neurodegenerative Disease.

The critical regulatory role of leptin in the neuroendocrine system has been widely reported. Significantly, leptin can improve learning and memory, affect hippocampal synaptic plasticity, exert neuroprotective efficacy and reduce the risk of several neuropsychiatric diseases. In terms of depression, leptin could modulate the levels of neurotransmitters, neurotrophic factors and reverse the dysfunction in the hypothalamic-pituitary-adrenal axis (HPA). At the same time, leptin affects neurological diseases during the regulation of metabolic homeostasis. With regards to neurodegenerative diseases, leptin can affect them via neuroprotection, mainly including Alzheimer's disease and Parkinson's disease. This review will summarize the mechanisms of leptin signaling within the neuroendocrine system with respect to these diseases and discuss the therapeutic potential of leptin.

Improving the Topside Profile of Ionosonde with TEC Retrieved from Spaceborne Polarimetric SAR.

Signals from spaceborne polarimetric synthetic aperture radar will suffer from Faraday rotations when they propagate through the ionosphere, especially those at L-band or lower frequencies, such as signals from the Phased Array type L-band Synthetic Aperture Radar (PALSAR). For this reason, Faraday rotation compensation should be considered. On the other hand, Faraday rotation could also be retrieved from distorted echoes. Moreover, combining Faraday rotation with the radar parameters and the model of magnetic field, we could derive the total electron content (TEC) along the signal path. Benefiting from the high spatial resolution of the SAR system, TEC obtained from PALSAR could be orders of magnitude higher in spatial resolution than that from GPS. Besides, we demonstrated that the precision of TEC from PALSAR is also much higher than that from GPS. With the precise TEC available, we could fuse it with data from other ionosphere detection devices to improve their performances. In this paper, we adopted it to help modify the empirically modeled topside profile of ionosonde. The results show that the divergence between the modified profile and the referenced incoherent scattering radar profile reduced by about 30 percent when compared to the original ionosonde topside profile.

Association between complement factor I gene polymorphisms and the risk of age-related macular degeneration: a Meta-analysis of literature.

AIM: To systematically review the association between complement factors I (CFI) polymorphisms and age-related macular degeneration (AMD) and to explore whether CFI polymorphisms are associated with AMD. METHODS: Meta-analysis of articles published from 1995 to January 2015 of articles involved with AMD and polymorphisms of the CFI gene. Eligible data were pooled in a Meta-analysis, analyzing using STATA software (version 12.0), Review Manager (version 5.2) and different models based on the heterogeneity of effect sizes. Egger's test, Begg's rank correlation methods were used to evaluate for publication bias. RESULTS: Thirteen articles were eligible, describing two loci polymorphisms of the CFI gene (of which 12 articles focus on rs10033900T>C and 3 articles focus on rs2285714C>T). For rs10033900T>C, the results of our study revealed that having a mutant allele C, TC, CC and TC+CC was associated with a decreased risk of AMD in all population groups studied (C versus T models, OR=0.84, 95%CI: 0.72-0.99, P=0.04; TC versus TT models OR=0.89, 95%CI: 0.88-0.99, P=0.04; CC versus TT models, OR=0.76, 95%CI: 0.60-0.98, P=0.03; TC+CC versus TT models, OR=0.81, 95%CI:0.65-0.99, P=0.04). We found that C allele were related to lower AMD risk in the Caucasian population by subgroup analysis, but there was no association with AMD under the allele and genotypes comparison in Asian studies. For rs2285714 C>T, the TC, TT genotypes contributed to a higher risk of AMD, compared with the CC carriers and TC+CC (OR=1.34, 95%CI: 1.09-1.63, P=0.004; OR=1.50, 95%CI: 1.25-1.80, P<0.0001). CONCLUSION: This Meta-analysis suggests that CFI rs10033900T>C and rs2285714C>T polymorphisms may contribute to AMD.

alpha-Crystallin downregulates the expression of TNF-alpha and iNOS by activated rat retinal microglia in vitro and in vivo.

PURPOSE: Inhibition of microglial activation has become an important strategy to attenuate neurotoxic damage to the central nervous system. We evaluated the effects of alpha-crystallin on the production of cytokines in lipopolysaccharides (LPS) and optic nerve injury-activated retinal microglia. METHODS: Microglia were collected from retinas of newborn rats, cultured and treated with LPS in vitro. Microglia were also activated by an optic nerve crush in vivo. Pretreatments with and without alpha-crystallin were performed in cultured cells, and by intravitreal injection in adult rats. Expression of tumor necrosis factor-alpha (TNF-alpha), nitric oxide (NO) and inducible NOS synthase (iNOS) were measured by RT-PCR, ELISA, Western blot and the nitrate reductase method. RESULTS: Activated microglia significantly upregulated TNF-alpha and iNOS mRNA expression and protein production in vitro. An optic nerve crush also increased expression of retinal iNOS and TNF-alpha protein. Treatment with alpha-crystallin in vitro and in vivo downregulated their expression. CONCLUSION: The protective effect of alpha-crystallin may be due to its effect on microglia via a downregulation in the expression and release of 2 key immune regulatory and inflammatory molecules: TNF-alpha and iNOS.

A comparison of LEDGFp52 and CNTF on the in vitro growth of rat retinal ganglion cell neurites.

Lens epithelium-derived growth factor (LEDGF) can be alternatively spliced to produce two isoforms-LEDGFp52 and LEDGFp75, however, LEDGFp52 has rarely been investigated. The LEDGFp52 protein or its monoclonal antibody was added to primary rat retinal ganglion cell cultures and their impact on neurite number and length, and the mRNA and protein expression levels of GAP-43, NF-L and MAP-2 quantified. LEDGFp52 was compared to the addition of ciliary neurotrophic factor (CNTF). LEDGFp52 protein significantly increased primary neurite growth compared to control conditions. In addition, the expression of GAP-43, NF-L and MAP2 genes and proteins were also significantly up-regulated. The positive action of the LEDGFp52 protein was similar to or more efficacious than CNTF. LEDGFp52 appears to be an important regulatory protein for the growth of cell processes.